Pediatric Hypersensitivity Pneumonitis 

  • Author: Harold J Farber, MD; Chief Editor: Michael R Bye, MD   more...
 
Updated: Mar 1, 2010
 

Background

Hypersensitivity pneumonitis (HP) refers to a group of disorders caused by a nonatopic immunologic response to an inhaled agent. In its acute or subacute form, hypersensitivity pneumonitis may be a cause of recurrent pneumonitis. In its chronic form, hypersensitivity pneumonitis may insidiously lead to pulmonary fibrosis and end-stage lung disease.

Severe acute or subacute flares can be life threatening,[1] and recurrent or chronic disease can lead to permanent, severe lung damage.[2] Although rare, fatal cases of chronic hypersensitivity pneumonitis have been reported in children.[3] Hypersensitivity pneumonitides are classically considered occupational illnesses and have colorful names reflecting the associated occupation. Some of these illnesses and their associated causes are as follows:[4]

  • Farm worker's lung - Thermophilic actinomycetes and other pathogens
  • Winemaker's lung -Botrytis cinerea
  • Coffee worker's lung - Coffee bean dust
  • Lifeguard's lung - Aerosolized endotoxin
  • Poultry worker's lung - Avian antigens
  • Laboratory worker's lung - Rodent antigens
  • Miller's lung - Wheat weevil
  • Woodworker's lung -Penicillium chrysogenum
  • Detergent worker's lung -Bacillus subtilis
  • Epoxy-resin lung - Phthalic anhydride
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Pathophysiology

Numerous organic and inorganic antigens can cause hypersensitivity pneumonitis. To cause pneumonitis, the antigen must penetrate into the small airways; therefore, its size must be within the respirable range (< 5 mm). Implicated antigens include avian (bird) antigens, mammalian proteins, fungi and fungal spores, bacterial antigens, and small-molecular-weight chemicals.[5] See Causes.

Immune responses

The immunopathogenesis of hypersensitivity pneumonitis has not been well characterized. An exuberant production of antibody (especially immunoglobulin G [IgG]) against the offending antigen is frequently identified. However, many patients with precipitating antibodies against antigens associated with hypersensitivity pneumonitis have no disease, suggesting that the precipitating antibodies by themselves are not the cause of the disease.[6, 7]

Although bronchoalveolar lavage (BAL) fluid (BALF) from adults with hypersensitivity pneumonitis reveals a decreased CD4/CD8 ratio of T lymphocytes and increased natural killer cells, this finding has not been consistently demonstrated in pediatric studies. Healthy children tend to naturally have a CD8 predominance, and this does not appear to be significantly altered in children with hypersensitivity pneumonitis. However, in all ages, lymphocytosis appears to be present.[8, 9, 10]

Various cytokines have been identified in acute hypersensitivity pneumonitides, but their role is poorly understood. These include interleukin (IL)-8, IL-12, tumor necrosis factor (TNF)-α and IFN-γ. IL-8 (a chemoattractant of neutrophils) is released by a cell line with properties of alveolar lung cells when stimulated by thermophilic bacteria.[11] High levels of IL-8 are released by alveolar macrophages in patients with acute hypersensitivity pneumonitis.[12] The levels of IL-12, IL-18, and TNF-α in BALF are greater in patients with hypersensitivity pneumonitis compared with controls.[13, 14] The levels of TNF-α became elevated in patients with acute farmer’s lung after an antigen challenge but were not elevated in unaffected farmers after antigen challenge.[15] .

A role for interferon-γ is suggested by the observation that interferon-γ knockout mice lack granulomatous inflammation in response to stimulation by thermophilic bacteria, whereas granulomatous inflammation develops in both knockout mice given interferon-γ replacement and wild-type mice.[16]

Hypersensitivity pneumonitis seems to be least common among active smokers of tobacco products. This relative infrequency might result from suppression of alveolar macrophage function.[17, 18, 19] However, a review of an outbreak of hypersensitivity pneumonitis among metalworkers suggested that low disease rates among tobacco smokers may reflect a high proportion of false-negative results instead of a truly low rate of disease.[20] Another study suggested that hypersensitivity pneumonitis may be insidious and is most often associated with low survival rates when it occurs in smokers.[21]

Genetics

Familial clustering of cases suggests a genetic predisposition, but a clear genetic locus has not yet been identified. Likewise, associations with different human leukocyte antigen (HLA) phenotypes have been suggested, but no clear or consistent pattern has emerged.[22, 23, 24] A study of BALF from children with hypersensitivity pneumonitis compared with healthy patients without lung disease showed an increase in lymphocytes expressing HLA-DR phenotype.[10]

Viral infections

Animal models have suggested that viral infections may play a role in triggering or augmenting hypersensitivity pneumonitis flares in genetically susceptible subjects.[25] Examination of BALF from persons with farmer’s lung showed respiratory viruses during acute exacerbations of farmer’s lung.[16]

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Epidemiology

Frequency

United States

The frequency in children is unknown.

International

Acute hypersensitivity pneumonitis in children is more common in areas where pigeon racing and pigeon breeding are popular. Chronic disease is more common in areas where caged birds are typical house pets.

Mortality/Morbidity

Mortality due to hypersensitivity pneumonitis in childhood is uncommon; however, fatal cases have been reported.[3] Significant morbidity can result if the child is not removed from the causative environment because flares of acute hypersensitivity pneumonitis can be severe and life-threatening.

Progression of chronic disease can lead to pulmonary fibrosis and end-stage lung disease. Severe pulmonary fibrosis with honeycombing and spontaneous pneumothorax as a consequence of chronic hypersensitivity pneumonitis has been described in an adolescent.[2] Such clinical picture is associated with high mortality rates.[26]

Age

See Mortality/Morbidity.

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Contributor Information and Disclosures
Author

Harold J Farber, MD  Associate Professor, Section of Pediatric Pulmonology, Baylor College of Medicine, Texas Children's Hospital

Harold J Farber, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Nidhy Paulose Varghese, MD  Assistant Professor of Pediatrics, Division of Pulmonology, Baylor College of Medicine, Texas Children's Hospital

Disclosure: Nothing to disclose.

Bettina C Hilman, MD  Consulting Staff, The Asthma and Allergy Center

Bettina C Hilman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Chest Physicians, American Heart Association, American Medical Association, American Pediatric Society, American Thoracic Society, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Girish D Sharma, MD  Associate Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center

Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Charles Callahan, DO  Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD  Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

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Anteroposterior chest radiograph reveals a right-sided tension pneumothorax with mediastinal shift to the left in a female adolescent with severe chronic hypersensitivity pneumonitis (HP) resulting from bird exposure. Radiograph reveals diffuse haziness and increased interstitial markings of the underlying lung. Reprinted with permission from Farber and Budson, 2000.
High-resolution chest CT scan in the same patient as in the previous image reveals ground-glass attenuation, areas of nodular attenuation, and a thickened interstitium. A chest tube is evacuating the pneumothorax. Reprinted with permission from Farber and Budson, 2000.
Axial high-resolution chest CT scan (1-mm section) obtained at the level of the third thoracic vertebra reveals a persistent right pneumothorax and diffuse ground-glass attenuation through both lung fields. Areas of nodular attenuation, a thickened interstitium, and small subpleural cysts are most prominent on the superior section. Reprinted with permission from Farber and Budson, 2000.
Photomicrograph of a lung biopsy specimen reveals marked interstitial inflammation with lymphocytic predominance and a multinucleated giant cell (hematoxylin-eosin stain, original magnification 40X). Reprinted with permission from Farber and Budson, 2000.
Photomicrograph of a lung biopsy sample reveals interstitial fibrosis with active interstitial inflammation (hematoxylin-eosin stain, original magnification 10X). Reprinted with permission from Farber and Budson, 2000.
Photograph reveals precipitin lines produced by means of Ouchterlony immunodiffusion assay. Central wells contain the patient's serum. Peripheral wells contain serum or droppings from various birds. Reprinted with permission from Farber and Budson, 2000.
Table 1. Commonly Described Causes of Hypersensitivity Pneumonitis[32]
Exposure Disease Source of Antigen
AvianBird fancier's lung, pigeon breeder's lung, poultry worker's lungFeathers, droppings, serum proteins, intestinal mucins, avian immunoglobulin A
AgricultureFarmer's lung, Bagasse (sugar cane) lung, mushroom worker's lung, potato riddler's lung, paprika slicer's lung, wine maker's lung Thermophilic actinomycetes, Aspergillus species, and other fungi in moldy hay or grains; moldy sugar cane; mushroom spores and thermophilic actinomycetes; moldy hay around potatoes, thermophilic actinomycetes, and others; Mucor stolonifer (on moldy paprika pods); B cinerea (noble rot on grapes)
Water-based systemsHumidifier lung, hot-tub lung, sauna taker's lung, lifeguard's lung, sewage pneumonitisAerosolized molds, endotoxins, mycobacteria, thermophilic actinomycetes, Penicillium species, others
Home environmentSummer-type pneumonitis, mold-contaminated walls, humidifiers, wallpaperTrichosporon species, mold contamination in older and/or water-damaged homes
ChemicalsChemical worker's lung, epoxy-resin lung, pyrethrum pneumonitisExposure to chemicals in manufacturing, laboratories, spray paints, heated epoxy resins, insecticides
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